K. Wiedemann et al., ATRIAL NATRIURETIC HORMONE INHIBITS CORTICOTROPIN-RELEASING HORMONE-INDUCED PROLACTIN-RELEASE IN MAN, Journal of Psychiatric Research, 29(1), 1995, pp. 51-58
Atrial natriuretic hormone (ANH) is found in heart myocytes, and also
in the CNS. The inhibitory action of ANH on the hypothalamic-pituitary
-adrenocortical (HPA) system has been established by in vivo and in vi
tro experiments, and could be of considerable importance: whereas seve
ral synergists to corticotropin-releasing hormone (CRH), the key hormo
ne of the HPA system, are characterized in the past, until now ANH see
ms to be the only peptide which counterbalances the effects of CRH at
the pituitary. As well as at the corticotroph, CRH has a stimulatory i
nfluence upon the lactotroph in vivo, and like ACTH and corticosteroid
s prolactin (PRL) is released in response to physical and cognitive ch
allenges. To test the hypothesis of whether ANH also inhibits the CRH-
mediated prolactin release a randomized, placebo-controlled, double-bl
ind study in 12 males aged from 25 to 30 years was conducted. With reg
ard to the diurnal variation of the HPA system activity we compared th
e prolactin release by 100 mu g hCRH during a 30 min infusion of place
bo, 150 mu g ANH or 3 IU arginine vasopressin in the morning (08 : 00
h) and evening (19 : 00 h). Evaluation of morning and evening effects
revealed that administration of hCRH led to a prompt rise of plasma PR
L concentration. Infusion of ANH resulted in a significantly reduced m
aximum increment of PRL compared to placebo (0.83 +/- 0.87 vs 2.85 +/-
1.57 ng/ml, ($) over bar X +/- SD, n = 12, p <.001). In addition, the
AUC values were significantly lower under ANH than in the placebo con
dition. Infusion of AVP did not significantly change the PRL response
to CRH vs placebo. These findings were similar both for morning and ev
ening application. Recent studies in animals showed that the CRH-media
ted release of prolactin can be antagonized by naloxone and dopamine r
eceptor blockers, pointing to an enhanced release of opioid peptides w
ith a consecutive inhibition of dopamine secretion. Whereas AVP mediat
ed effects were not observed, ANH seems to interact in this regulatory
cascade. However, our study could not determine whether indirect inhi
bitory effects upon CRH-mediated opioid secretion or direct effects up
on dopamine release are responsible for the present findings.